PANEL DISCUSSION
MANAGEMENT OF PCOS - WOMB to TOMB
MODERATOR : Sharda Jain
PANELISTS : Dr.Chitra setia
Dr Puneet Arora
Dr. Ila Gupta
Dr. Rupam Arora
Dr. Archana Sharma
Dr. Sangeeta Gupta
Dermatologists
Dr. V.K. Upadhyay
Dr. S. Kandhari
2. MANAGEMENT OF
- WOMB to TOMB
HELD ON 10/10/2014
At Wood Apple
NEW DELHI
Dr. Sharda Jain
Organized by Delhi Gynaecologist Forum / Sheild H. Care
PANEL DISCUSSION
PCOS
3. MANAGEMENT OF PCOS
WOMB to TOMB
MODERATOR : Sharda Jain
PANELISTS : Dr.Chitra setia
Dr Puneet Arora
Dr. Ila Gupta
Dr. Rupam Arora
Dr. Archana Sharma
Dr. Sangeeta Gupta
Dermatologists
Dr. V.K. Upadhyay
Dr. S. Kandhari
5. IMPORTANCE OF PCOS
Womb to Tomb
It is NOT A DISEASE, it is a syndrome with
varied presentations
PCOS has a CONTINUUM SPECTRUM
starting from the EARLY PREPUBERTAL
YEARS and continuing after Menopause
S/S peak through 2nd
/ 3rd
decade of life
But Does not become quiescent till her death
6. Why has journey
From Womb To Tomb
• Above average (LFD) or
low birth weight for
gestational age.
• Premature Adrenarche,
• Atypical Sexual Precocity
Birth
Prepubertal
PCOS
7. PCOS
PCOS is condition which can effect
• women menstrual cycle,
• Fertility
• Her appearance (obesity, Acne, Hirsutism)
• Hormones / Depression
• Has long term health sequelae.
(Morbid Co-morbidities)
8. * Obesity * Dyslipidemia
*DM *Hypertension
• Acanthosis nigricans , skin Tags
• Fatty liver
• Sleep apnoea
INSULIN Resistance is the key …….finding
Endometrial Carcinoma
Why has journey
From Womb To Tomb
PCOS
4 Sibling
10. EPIDEMIOLOGY
Yes, Both things are working
• There is a increase in incidence of PCOS in
adolescents
• Secondly because diagnosis has improved from
NIH-(1990) – TO ROTTERDOM(2004) – TO AES-
PCOS SOCIETY DIAG.CRITERIA (2009)
– many more cases are picked –up now
11. Improvement in
Diagnosis of PCOS over the years
NIH (1990)
1. Oligo ovulation
2. Hyperandrogenism and / or hyperandrogenemia
(with exclusion of related disorders)
ESHRE /ASRM (Rotterdam 2003)
To include TWO OUT OF THREE of the following:
1. Oligo – or anovulation
2. Clinical and / or biochemical signs of hyperandrogenism
3. Polycystic ovarian (with exclusion of related disorders)
12. Improvement in
Diagnosis of PCOS over the years
AES – PCOS (2009)
1. Hyperandrogenism : hirsutism and / or
hyperandrogenemia and
2. Ovarian dysfunction : oligo – anovulation and / or
polycystic ovaries and
3. Exclusion of other androgen excess or related
disorders
13. PCOS
Definition
1990 - 2009
Hyperandrogenism
(Clinical or
Biochemical )
Oligo- menorrhea
or
Oligo-Ovulation
Polycystic Ovaries
on USG
NIH (1990) yes yes no
Rotterdam
(2003)
yes Yes
2 of the 3 criteria
yes
AE-PCOS
Society
(2009)
yes Yes
1 of 2 criteria
yes
Diagnosis of Polycystic Ovarian Syndrome
14. Incidence of adolescent
PCOS
IF WE USE STRICTLY
NIH criteria = 6-8%
Rotterdam criteria = 15-25%
In Indian Asian Urban Community– this
number is more & seems to be rising
for reasons unknown ??
15. Prevalence of PCOD In India
30-36% Girls
Indian j pediatr.2012 jan;79suppl 1:s69-73
J pediatr adolesc gynecol.2011 Aug;24(4): 223-7
16. Near 18-20% (1 in 5) girls going to private
schools in Delhi have PCOS (LPS)
OBESE – 50% (over weight , BMI>24 & obese >27)
MENSTRUAL PROBLEMS – 60%
Delayed Periods Most Common
Heavy Menstrual Bleeding – 20%
HIRSUTISM – 60-70%
ACNE – 30%
DGF Survey of 2 schools 2004
EXPERIENCE
17. What are the Conditions
That May Mimic PCOS ?
Q 2
D/D
19. • Thyroid disorders
• Hyperprolactinemia
• Cushing’s syndrome
• Late onset congenital adrenal hyperplasia (CAH)
• Basal morning 17-OHP
• Ovarian and adrenal tumors DHEAS
• WHO I &III –FSH,LH,E2
• Syndromes of severe insulin resistance(HAIRAN syn)
Sr.TSH,Sr.PrlSr.TSH,Sr.Prl
Dexa supression testDexa supression test
What are the conditions
that may mimic PCOS ?
21. Any Genetic or Familial Basis ?
• FAMILY Clustering is
known :
Risk of PCOS
• 40% - if her sister is having
PCOS
• 20% - if her mother suffered
from PCOS
• N = 5-10%
GENETIC ETIOLOGY NO LAST WORD AS YET
22. Genetic & PCOS
AUTOSOMAL DOMINANT pattern of
inheritance
Several genes namely
CYP 17
CYP11A
CYP21,
SHBG
Insulin receptor
NO
CONCLUSIVE
RESULT
TILL DATE
24. Testosterone level
LH and FSH High LH & low FSH is seen in 60% cases
only
TSH
Prolactin level
Fasting glucose level or 2 hr 75 gm OGTT
Lipid profile, including total, LDL,HDL
17-hydroxyprogesterone level*
*--(Fasting level to r/o CAH)
DIAGNOSTICS – BLOOD TESTS
25. Which tests should be done before starting
insulin sensitizers – fasting / PP blood sugar,
insulin, Glycosylated Hb?
DIAGNOSTICS – BLOOD TESTS
before METFORMIN
Q4B
26. • using fasting & 2 hrs blood sugar levels
following 75gm glucose load is all that is
needed
DIAGNOSTICS – BLOOD TESTS
Insulin Levels are Really Not Needed for
diagnosis of PCOS
Category Fasting 2hrs PP
Normal <100 mg/dl <140 mg/dl
Impaired <100-126 mg/dl > 140 -199
NIDDM Over 126 Over 200
28. USGUSG CRITERIACRITERIA ofof
POLYCYSTIC OVARIAN MORPHOLOGYPOLYCYSTIC OVARIAN MORPHOLOGY
• Presence of 12 or more follicles in eachPresence of 12 or more follicles in each
ovary , 2 - 9 mm in diameter and orovary , 2 - 9 mm in diameter and or
increased ovarian volume > 10 mlincreased ovarian volume > 10 ml
Or 10 cmOr 10 cm33
• Single ovary is sufficientSingle ovary is sufficient
to diagnose PCOSto diagnose PCOS
• Optimal time forOptimal time for
ultrasound (TVS) is D3 – D5ultrasound (TVS) is D3 – D5
29. • It is a fact that PCOM ie POLYCYSTIC
OVARIAN MORPHOLOGY is present in
20 -35% girls with NORMAL menstrual
cycles &
• In Contrast there are patients of TYPICAL
PCOS who do not have PCOM on ultrasound.
Q5.
PCO, PCOM & PCOS
30. What are the PHENOTYPES in
PCOS & what is there importance ?
Q 6.
31. Four Different Phenotypes of PCOS are
now identified
• TYPE A: hyperandrogenism, chronic anovulation and<
polycystic ovaries.
• TYPE B: hyperandrogenism and chronic anovulation.
• TYPE C : hyperandrogenism and polycystic ovaries
• TYPE D : chronic anovulation and polycystic ovaries
Hyperandrogenemia is the
Hallmark of PCOS
33. Three Commonest Presentation are
• MENSTRUAL DISORDERS when they consult
gynaecologists
•OBESITY when they consult endrocrinologists
•HISUITISM & ACNE when they consult dermatologist
Ans.
SYMPTOMS/ Management
current options
Co-operations / Coordination
among specialists is needed
in Adolescents –Management Is Specific To Clinical
Symptoms
35. Symptoms & There Frequency
in PCOS in Adolescents
Menstrual Cycle disturbance – 70%
- Oligomenorrhoea 50%
- Amenorrhoea 10%
- Abnormal heavy bleeding 10-15%
Hyperandrogenism 70%
Acne – 30 - 40%
Hirsutism 70%
Alopecia 10% as seen by Gynaecologits
Acanthosis Nigricans 1-3% lean & 20% obese
OBESITY 50- 60 %
NORMAL MENSTRUATION 20%
* INFERTILITY - 70% * EARLY PREGNANCY LOSS 50-60%
36. Q 8(A)
What is the Pattern of MENSTRUAL
IRREGULARITY in Adolescent PCOS
Q 8(B)
Why MENSTRUAL IRREGULARITY in
Adolescent PCOS needs treatment ?
37. DELAYED PERIODS is most common
presentation
Other Presentations are:
• Withdrawal bleeding only
• Absent periods
• Heavy menstrual bleeding or
• Menometrorrhagia with Anemia
Ans 8(A)
What is the Pattern of Menstrual
Irregularity in Adolescent PCOS
•20% PCOS have
• normal cycles
Obese
80%
Lean
30%
38. Ans 8(B)
Why MENSTRUAL IRREGULARITY in
Adolescent PCOS needs treatment ?
• Menstrual irregularity in adolescent
PCOS needs treatment because
chronic anovulation increases the risk
of developing Endometrial
Hyperplasia , which is associated with
Endometrial Carcinoma if not
monitored.
• In addition , anemia can result from
dysfunctional DUB or menorrhagia
Treatment IS Discussed LATER
39. • It is well accepted that If
menstrual
Irregularities persist for 2
years
After Menarche,
Then The Risk for PCOS is
Extremely High (70% of
Cases)
40. PCOS remains largely
UNDIAGNOSED as irregular
menses after menarche for 2
years & acne is commonly
seen in adolescents
• Transabdominal ultrasound
resolution has poor sensitivity
to diagnose PCOS
TVS is recommended
41. Q-9
COSMETIC CONCERNS
Question to Dermatologist
Dr. V. K. UPADHYAY / Dr. S
KANDHARI
WHAT ABOUT INCIDENCE OF
ALOPECIA & ACANTHOSIS
NIGRICANS IN ADOLESCENTS ?
42. COSMETIC CONCERNS
• Alopecia 10% as seen by Gynaecologists
(Dermatologist feel - Alopecia
is not all that uncommon & is
around 20%)
HAIR
LOSS
HAIR
LOSS
AcanthosisAcanthosis
Acanthosis Nigricans
1-3% lean & 20% obese
43. Is treatment for hirsutism based on
Ferring Gallway SCORING?
Q10(A).
COSMETIC CONCERNS
HIRSUTISM , ACNE, ALOPECIA
45. Ferring Gallway Scale
This model quantities the extent of hair
growth in nine key anatomic sites: the
hair growth is graded using a scale from
0 (no terminal hair) to 4 (maximum
growth), for a maximum score of 36
A score of 8 or more indicates the
presence of androgen exces.
However, we do not use it in day to
day practice to grade our patients
46. what all tests are needed to
diagnose HYPERANDROGENEMIA?
Q10 (B).
COSMETIC CONCERNS
HIRSUTISM , ACNE, ALOPECIA
47. What All Test Are Needed To Diagnose
Hyperandrogenism
(Hirsutism, acne, alopecia)
Free Testosterone &
% Free Androgen index have NO ROLE in
diagnosis. It is 10 times costly & is not standard in all
labs.
• ANDROSTENADIONE-NO ROLE
BIOCHEMICAL TESTING
Total Testosterone
& 17 – hydroxyprogesterone level to
R/O late onset CAH is all that is needed
48. NORMAL VALUES OF SERUM ANDROGENS
Testosterone (Total) 20-80 ng/dl
DHEAS 100-350 mg/dl
17 – hydroxprogesterone
(Follicular phase)
30-200 ng /dl
Over 800 diagnostic of
adult onset CAH
49. SUDDEN ONSET of these symptoms suggests
other D/D
* Cushing’s syndrome
* Adrenal or ovarian tumor.
Q10C
Hirsutism – Virilisation
50. Does ACNE require systemic treatment
or only topical is sufficient?
Q11
COSMETIC CONCERNS
51. ACNE
• Grade 1: Acne are classified
non inflammatory
• Grade 2: Inflammatory
• Grade 3 : Combination of
above (Severe)
• Topical Retinoids
•Antimicrobial aqents +
•topical ratinoids
TREATMENT MEDICAL ENDOCRINE THERAPY +
TOPICAL / ORAL RATINOIDS
52. Management Topical
Retinoids1. Apply the preparation over the whole affected
area and not just spot application
2. Apply the product very miserly as Acne
treatments are often irritating and drying
3. Excessive washing of face is to be avoided as it
further aggravates the irritation
4. Stop application the moment excessive drying
or irritation develops
5. Cream based applications should be preferred
as they reduce the concomitant dryness
ACNE GRADE - I
53. Systemic – Management
is needed for infected or severe acne
• ORAL ANTIBIOTICS – Minocycline,
Doxycycline, Azithromycin,
CEPHALOSPORINS
• Isotretenoin – 0.5 -1 mg/ Kg body
weight. Cumulative dose of 120 – 150
mg /Kg over a period of 6 – 9 months.
• Low dose OCP
Acne / Grade II & III
54. Hormonal Therapy in Acne
– Recalcitrant acne (severe Acne)
– Acne not responding to topical /oral
Isotretenoin
– Co- prescribed with Isotretenoin
•OCP
•6-9 MONTHS
•Any pill
55. Acne Treatment – Other Modalities
• Chemical peels
• Comedon removal
• IPL
• Cryotherapy
• Microneedling
• Use of steroids
Good Dermatologist
help is needed.
Gynaecologist can’t
treat on there own
56. How common is ALOPECIA ?
Treatment ?
Q12
COSMETIC CONCERNS
57. Alopecia
Dermatologist feel that it is not all that uncommon
• Diffuse thinning
With preservation
of frontal line
• Bitemporal
recession
CAUSE
• Decrease in 5a
reductase -
• in DHT
Incidence
in adolescent PCOS
DERMATOLOGIST To Be Care
60. TREATMENT - HIRSUTISM
• All combination OCPs are effective
• OCPs decrease androgen levels by
suppressing LH and stimulating sex
hormone binding globulin (SHBG).
• It takes almost 6 months when decrease
growth of hair is noted.
•OCPs with low androgenic
Progestins (norgestimate, desogestrel)
may be Most effective for acne and hirsuitism
61. Hirsutism Treatment
• METFORMIN perse are not needed
– To reduce hirsuitism.
– Spironolactone 100mg twice daily (max dose
200 mg/day).
– A full clinical effect may take 6 months or
more
– After a periods of time, maintenance dose of
25-50 mg daily.
Anti ANDROGENS (RECEPTOR BLOCKERS)
64. Q -14 C
TOPICAL HAIR GROWTH RETARDANTS
• EFFORNITHINE HYDROCHLORIDE CREAM are
effective & take almost 3 months to show effect.
Dosages & Applications
• Remove the heir from the affected areas and wait for minimum 5
minutes
• Apply a thin layer of hinder cream to the affected areas of the face
and adjacant involved areas under the chin
• Rub in thoroughly
• The treated area should not be washed for 4 hours
• Cosmetics and sunscreens may be applied over the treated areas
after the cream has dried
• To be used twice daily at least 8 hours apart
• For optimal results, use hinder fo a minimum of 6-12 months along
with other methods of hair removal
65. Q -14 D
Great TIPS on Solution of Hirsutism
• Temporary Methods – Remove the hair
shafts but leave the hair follicle intact.
Example – waxing, shaving, depilatory
creams & plucking
The process needs to be repeated indefinitely.
Though cheap & effective, are time consuming,
repetitive and often lead to pigmentation and
thickening of skin.
OCP & ALDACTONE ARE NEEDED
66. ELECTROLYSIS IS GOING OUT
(Burns / Scarring)
LASER THERAPY is not permanent.
Repeated sittings may be needed
Q -14 D
Great TIPS on Solution of Hirsutism
OCP & ALDACTONE ARE NEEDED
67. Which COC is most preferred?
Containing
• Levonorgestrel / Desogestrel
• Cyproterone acetate
• Drospirenone
Q -15.
CHOICE OF COC
Menstrual Irregularity / Hirsutism / Acne
68. CHOICE of COC
ANY LOW DOSE COC CAN BE GIVEN
• OC’s containing progestins such as NORGESTREL
/ LEVONORGESTREL / DESOGESTREL are preferable.
•DROSPIRENONE HAS NO ADVANTAGE
• If HIRSUTISM is a problem then
Cyproterone Acetate (CPA) is preferred.
69. Two Types OF OCPs
Desogestrel 0.15 mg + EE 30mcg(novelon)
Desogestrel 0.15 mg + EE 20mcg( femilon)
Cyperoterone acetate
(EE 30 mcg + C 2 mg - Diane35)
Drosperinone- (EE 30 mcg + D 3 mg -Yasmin)
NON ANDROGENIC PROGESTOGENS
ANTIANDROGENS WITH PROGESTATIONAL ACTIVITY
70. Q 15 B
What are the
DRAWBACK OF OCP
IN PCOS
• Menstrual Problem
• Hirsutism
71. What are the DRAWBACK OF OCP
IN PCOS
• Cause salt & water retention making weight
loss more difficult.
• In permenarcheal girls with short stature who
have open epiphyses, OCPs are
contraindicated bcz OCPs contain growth –
inhibitory amounts of estrogen
• In Incompletely mature girls - increase risk of
post pill amehhnoria
• VTE with OCP is primarily related to dose &
duration of estrogen use & progesterone like
DROSPERINONE (Twofold increase)
73. OCPs FOR HOW LONG ??
in Adolescents PCOS?
Hirsutims / Menstrual
By three months the bleeding problems gets
stabilized & by six month markedly decrease
growth hair is noticed.
74. As a general rule, OCPs should be
continued until the girls is gynaecologcally
mature (Five years postmenarcheal) or
has lost substantial amount of excess weight.
75. Gynaecologists are confused & use it for
variable periods but
sr. DERMATOLOGISTS feel it should not be
discontinued unless girls wants to become
pregnant .
DURATION OF TREATMENT with
OCP is Controversial
76. Q16.
ETHINYLESTRADIOL – HOW MUCH in
OCP?
What is the patient profile for
choosing COCs containing 35, 30,
20 mcg ethinylestradiol ?
77. Low Dose COC pill is the choice
(<35 ug EE is the choice).
In adolescent people start with EE 20 ug pill
– if BTB – occurs, higher dosage pill is used
ETHINYLESTRADIOL in OCP
– HOW MUCH?
78. Q-17
CHOICE OF PROGESTIN in OCP
What is the patient profile for
choosing the type of
PROGESTERONE in COCs?
79. Safety of the pill is most important
Like venus thromboembolism , mycardial
infaction & cancer etc.
CHOICE OF PROGESTIN
80. SAFETY of OCP is key
• Non Androgenic Progestogens
Desogestrel 0.15 mg + EE 30mcg(novelon) ,
Desogestrel 0.15 mg + EE 20mcg( femilon)
•Antiandrogens with progestational activity
• Cyperoterone acetate
• (EE 30 mcg + C 2 mg - Diane35)
Drosperinone DVT twofold increase (BMJ)
Noethindrone
Norgestril / Levonorgestril Low DVT
1st
Gen.
2nd
Gen.
DVT
?
Drosperinone- (EE 30 mcg + D 3 mg Yasmin)
81. Q18.
CONCERNS WITH COC
Q. What are common complaints with the use of
COCs?
* HYPERTENSION * WEIGHT GAIN * ACNE
82. HYPERTENSION – in few 10 mm rise of BLOOD
PRESSURE may be there which settles once the drug is off
WEIGHT GAIN is not the complication with low dose
COC pills.
ACNE : Infact OCP is the treatment. We preferred pill with
Antiandrogens with progestational activity
CONCERNS WITH COC
84. • MICRONIZED PROGESTERONE
(100 to 200 mg given orally at bedtime)
• MEDROXPROGESTERONE ACETATE
(10mg given orally at bedtime)
can be used for 7 to 10 days out of each month of cycle.
SIDE EFFECTS of progestin include * mood symptoms
(depression) * Bloating * Breast soreness
Role of Progestin in Menstrual
Irregularity
Patients must be informed that oral progestin
Prescribed in this manners (i.e. 7 to 10 days each month)
is not a means of contraception
85. How frequently do you see IR in your
PCOS patients?
• Why we are worried ?
• Various syndrome with IR
• Special signature of IP
• Role of metformin
Q20
INSULIN RESISTANCE
?
86. Ans. In Research situations IR is seen in
good 65 to 70% patients among whom
70 to 80% are obese (BMI > 30) & 20 to
25% are normal weight.
It is the biggest risk factor for type 2 DM
and cardiovascular disease
Ref.http:www.uptodate.com
INSULIN RESISTANCE
87. You should Know
Insulin Resistance is present
Various Clinical Syndrome
• Type 2 diabetes
• Cardiovascular disease
• Essential hypertension
• Polycystic ovary syndrome
• Non-alcoholic fatty liver disease (NASH)
• Certain forms of cancer -
breast,colon,liver,prostate
• Sleep apnea
All are interrelated
88. • SKIN : Acanthosis nigricans (darkly shaded skin in the
flexures of the neck , axilla, or groin – IR/DM)
Significant Findings Insulin Resistance
which gynaecologits should always note
Skin tags – IR/DM
10 %
Acanthosis nigricans
Over 20% obese
5% in lean
90. Gynaecologist are Not Clear and
use metformin Left & Right
Both ESHRE & ASRM consensus is that
no clear role for insulin sensitizing in
management of PCOS except in patients
with glucose or type 2 diabetes
Therefore, on current evidence -
metformin is not a first line treatment of
choice in the management of PCOS for
any clinical manifestation
91. Insulin sensitizers like metformin is
used in patients with impaired
glucose tolerance patients & not
otherwise
INSULIN RESISTANCE
92. • IMPAIRED Glucose Tolerance /
Type 2 Diabetes
– Up to 40% of women with PCOS have impaired
glucose tolerance (IGT).
– Risk of IGT and Type 2 Diabetes Mellitus (DM) is
increased in both obese and non-obese women
with PCOS.
– Retrospective studies have shown 2 to 5 fold
increase of type 2 diabetes in women with PCOS.
Importance &Importance &
How to Diagnose Insulin Resistance –How to Diagnose Insulin Resistance –
Just Do Fasting Glucose & 75 gm 2 hrs oral GTTJust Do Fasting Glucose & 75 gm 2 hrs oral GTT
93. Q(A) In patients who do not respond to one
COC, do you change the COC (consisting of
another progestin) or shift them to or add an
insulin sensitizer?
Q(B). Metformin / Myoinositol
Q21.
Place of INSULIN SENSITIZERS in- YOUR
OPINION?
94. METFORMIN—PRESENT ROLE
• Although there had been widespread enthusiasm to use
metformin left & right – but clinical data no longer
support this approach
• Use of metformin in PCOS
should be restricted to those
patients with glucose intolerance
ESHRE/ASRM-Sponsored PCOS Consensus
Workshop *,2007, Thessaloniki, Greece
95. Dose of Metformin
• When metformin is given , therapy is started
with 500 mg daily before the evening
meal, with an increase in the dose by 500
mg per week to the effective dose of 1500
to 2000 mg daily , as tolerated .
• The greatest dose (1500 to 2000) often
are better tolerated when divided into two
daily doses or when given in an extended
release form
97. Q 22
PREGNANCY & PCOS
If the female wishes to conceive, when
would you advise
her to stop taking the insulin
sensitizers and / or COCs?
98. COCs need to be stopped, FOLIC ACID
started & drugs for ovarian stimulation to be
used.
CLOMIPHENE CITRATE IS
Widely used Simple to use
Minimal side effects Cost effective
PREGNANCY & PCOS
101. FIRST LINEFIRST LINE
CLOMIPHENE CITRATE
SECOND LINESECOND LINE
LOD/GONADOTROPINS
THIRD LINETHIRD LINE
IVF
The Thessaloniki ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group March
2–3, 2007, Thessaloniki, Greece. Human Reproduction 2008
RR
EE
SS
II
SS
TT
AA
NN
CC
EE
RR
EE
SS
II
SS
TT
AA
NN
CC
EE
FF
AA
II
LL
UU
RR
EE
THESSALONIKI CONSENSUS ON INFERTILITY
TREATMENT IN PCOS, GREECE 2007
102. Q (a) Ovulation induction aim
(B) First & second line management of
infertility in women with PCOS?
(c) Role of LOD
(D) Role Luteal phase support
(E) OHSS
PCOS & INFERTILITY
103. Suggested a step by step approach to
ovulation induction in women with PCOS
Steps Approach
1 If BMI is elevated - loss at least 5% of current body
weight
2 Ovulation induction with clomiphene citrate
3 Metformin in combination with clomiphene
citrate in CC resistant cases or
BMI > 27 ???
4 Gonadotropin Therapy (OHSS / multiple
pregnancy)
5 Laparoscopic Ovarian Drilling
6 IVF ± Metformin Insulin sensitizer in combination with
gonadotropin therapy to decrease OHSS
104. Goals of Ovulation induction
in IUI / IVF
Minimize Complications &
Risk
AIM
Ideal Outcome
Singleton live
Birth at term
Cycle
Cancellation
Multiple
Pregnancy OHSS
105. 1. First Line Management
Clomiphene is drug of Choice
2. In CC Resistant cases
metformine has a role
3. 2nd
line treatment Lap. Ovarian
drilling has a role for women who
can’t came for closed follow – up
pregnancy role is 50%
4. Gonadotrophines in PCOS have
promise, but OHSS & multiple
pregnancy, should never before
gotten complication
•Tamoxiphene
people have just
staring using it
•Letroz is
banned in india
•Metformine role
dealt
106. The Truth is that
OHSS MUST
BE PREVENTED RATHER than
treated
108. Metformin may be added to CC in
women with clomiphene resistance who
are older and have visceral obesity (I-
A)
SOGC guidelines, 2010
METFORMIN
ROLE IN INFERTILITY
109. Q 24
PREGNANCY & PCOS
What is the line of treatment in women
with PCOS who have
CONCEIVED NATURALLY ?
110. • PCOS patients have high chance of
miscarriages so they need TLC +
micronised vaginal progesterone
• If they have conceived while taking
Metformin - it has to be continued for 3
months. This decreases miscarriage
rate.
• Few caution throughout pregnancy
PREGNANCY & PCOS
111. Q 25
Can we do
LAPAROSCOPIC OVARIAN DRILLING
in ADOLESCENTS who do not respond to
OCP
Not
Recommended
except for infertility problems
112. Q26.
LONG-TERM COMPLICATIONS
Q. Are the women sensitized to the
long- term complications of PCOS?
Infertility, Diabetes, Cardiovascular diseases,
Cancer…
113. COUNSELING IS IMPORTANT AT THE FIRST VISIT
detailing them of short term & long term
consequences.
It helps them in REDUCING WEIGHT, strictly
following life style modifications & become
proactive about conception & metabolic
disorders timely.
LONG-TERM COMPLICATIONS
114. Consequences of Polycystic
Ovarian disorders
Short Term consequences
• Obesity
• Infertility
• Irregular menses
• Abnormal lipid levels/ Hypertension
• Hirsutism/acne/androgenic alopecia
• Glucose intolerace / acanthosis nigricans
• Increase early pregnancy loss / GDM
Long – Term consequences
• Dibetes mellitus
• Endometrial cancer
• Cardiovascular disease
115. The Most
Common
Endocrine
disorder
In women
Symptoms may
Include chronically
irregular and / or
Absent or delayed
periods
Symptoms may
include facial
hair , central
obesity and
acne
Let untreated it
may lead to
Heart
Disease
Left untreated,
it may lead to
Uterine cancer
Leading cause
of
Infertility
P C O D
Long Term Complications &
Consequences
116. Counseling also helps them to get
regular screening / monitor from time to
time detect problems early.
•Infertility ,
•Diabetes
•Cardiovascular disease,
•Endometrial Cancer..
Q27
Counseling
117. Q28.
CANCER
in women & PCOS
Would you like to comment on
a) Endometrial Cancer
b) Breast cancer in PCOS
c) Your Pregnancy Experience
118. Ans. 28 A
Endometrial Cancer in PCOS
• Gynaecologists should not forget that
there is 3 fold increase in incidence of
endometrial cancer.
• There Should be screening &
monitoring for the same from time to
time with TVS & EB
119. Ans. 28 B
PCOS & Breast Cancer ??
Limited data exist that Do Not Support the
conclusion that women with PCOS are a
increased risk for BREAST CANCER.
121. OBESITY & PSYCHOSOCIAL
HEALTH in WOMAN
1. Poor body image
2. Social stigmatisation (‘a laughing
matter’)
3. Lower education levels
4. Lower rates of marriage
5. Lower socio economic levels
Neglected Area
122. Management of Obesity
in general
1st
LINE OF MANAGEMENT : Lifestyle changes like
modification of diet , physical activity and daily habits
2nd
line of Management : introduction of pharmacotherapy
for patients with BMI above 24 with co – morbidities and
BMI above 27.5 with no co- morbidity
BARIATRIC SURGERY : may be an option for treatment
of morbid obesity (BMI > 32.5) when diet and exercise
do not work
1
2
3
126. Q 31
Prevention of Endometrial Ca.
Monitoring of PCOS patients to prevent
occurrence of Endometrial Carcinoma
Guidelines
• Frequent TVS
• Endometrial Sampling
• Progesterone for periods
127. • TAILOR MADE THERAPY in
Adolescent PCOS is our attempt
in this panel discussion
CONCLUSION
128. RULE OUT Diagnosis:
Pre-Diabetes Fatty Liver
Diabetes type II Hyperlipidemia
Insulin Resistance Hypo-Thyroidism
Metabolic Syndrome Vitamin-D Deficiency
Cancer screening – Endometrial Ca.
CONCLUSION
130. More & More PCOS CLUBS
should be formed
To shoot
Information for
teens & young
PCOS patients on
its
various aspects
131.
132. www.delhigynaecologistforum.com
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Editor's Notes
Testosterone needed if considering treatment with antiandrogen for hisuitism as levels can then be followed.
DHEAS not needed.
Fasting morning 17-hydroxyprogesterone
Levels &gt; 800 ng/dL (8ng/ml) highly suspicious for late-onset congenital adrenal hyperplasia (CAH)
Levels between 200-800 ng/dL (2-8ng/ml) unclear
Levels &lt; 200 ng/dL (2ng/ml) usually no CAH
A ratio of less than 4.5 of fasting glucose to insulin levels correlates significantly with insulin resistance and has been studied for use as a screening test in obese patients with PCOS. Suggested only in selected patients. Information from Legro RS. Polycystic ovary syndrome: current and future treatment paradigms. Am J Obstet Gynecol 1998;179:S101-8.
Increased SHBG leads to decreased free testosterone
Yasmin (drospirenone/ ethinyl estradiol) contains an anti-androgen roughly equivalent to spironolactone 25mg.
Orthotricyclen with norgestimate has FDA approval fot the tx of hirsuitism but most experts believe all the 3rd generation ocps to be as efficacious for hirsuitism as they all have less androgenic progestins.
All non-FDA approved indications!
These androgen receptor blockers can be used in combination with ocp in cases when ocp alone is not adequate
Testosterone levels can be followed to show efficacy with goal &lt; 60.
It is postulated that topical eflornithine HCl irreversibly inhibits skin ODC (ornithine decarboxylase) activity which slows the rate of hair growth. Marked improvement was seen consistently at 8 weeks after initiation of treatment and continued throughout the 24 weeks of treatment. Hair growth approached pretreatment levels within 8 weeks of treatment withdrawal. Vaniqa has only been studied on the face and adjacent involved areas under the chin of affected individuals. If skin irritation or intolerance develops, direct the patient to temporarily reduce the frequency of application (e.g., once a day). If irritation continues, the patient should discontinue use of the product.Apply a thin layer of Vaniqa to affected areas of the face and adjacent involved areas under the chin and rub in thoroughly. Do not wash treated area for at least 4 hours. Use twice daily at least 8 hours apart or as directed by a physician. IV vaniqa is used to treat sleeping sickness caused by Trypanosoma brucei gambiense.
Cost $52.90 for 30gm tube.
Propecia (finasteride), a synthetic 4-azasteroid compound, is a specific inhibitor of steroid Type II 5α-reductase, an intracellular enzyme that converts the androgen testosterone into 5α-dihydrotestosterone (DHT).
Cost about $54 for 30d supply.
Flutamide warning-Serum transaminase levels should be measured prior to starting treatment with flutamide. Flutamide is not recommended in patients whose ALT values exceed twice the upper limit of normal. Serum transaminase levels should then be measured monthly for the first 4 months of therapy, and periodically thereafter. Liver function tests also should be obtained at the first signs and symptoms suggestive of liver dysfunction, e.g., nausea, vomiting, abdominal pain, fatigue, anorexia, &quot;flu-like&quot; symptoms, hyperbilirubinuria, jaundice or right upper quadrant tenderness. If at any time, a patient has jaundice, or their ALT rises above 2 times the upper limit of normal, flutamide should be immediately discontinued with close follow-up of liver function tests until resolution. Cost $374 for 3 month supply. In animal studies, flutamide demonstrates potent antiandrogenic effects. It exerts its antiandrogenic action by inhibiting androgen uptake and/or by inhibiting nuclear binding of androgen in target tissues or both. One metabolite of flutamide is 4-nitro-3-flouro-methylaniline. Several toxicities consistent with aniline exposure, including methemoglobinemia, hemolytic anemia and cholestatic jaundice have been observed in both animals and humans after flutamide administration. In patients susceptible to aniline toxicity (e.g., persons with glucose-6-phosphate dehydrogenase deficiency, hemoglobin M disease and smokers), monitoring of methemoglobin levels should be considered. There is a drug interaction with warfarin.
Spironolactone- competitively binds androgen receptors as well as inhibits alpha-reductase activity.
Concomitant administration of potassium-sparing diuretics and ACE inhibitors or nonsteroidal anti-inflammatory drugs (NSAIDs), e.g., indomethacin, has been associated with severe hyperkalemia. Cost $82 for 100 tablets of 50 mg.
75% of PCOS women have IR
Breast cancer patients found to be hyperinsulinemic and best data to support IR association.
Prostate, colon and liver cancers also more common in obese pts with type 2 DM or pts with increased insulin levels.
Up to 50% of all pts with essential HTN are IR.
Metabolic syndrome is defined to capture subset of people with IR at risk for CVD so as to be a practical dx to address CVD risk but IR syndrome may be better way to describe etiology and more studies are looking at IR.
insulin resistance is not a disease but the description of a physiologic state that greatly increases the chances of an individual developing several closely related abnormalities and associated clinical syndromes.
PCOS pts may have IR and it is not obesity dependent.
A prospective study of 254 women with PCOS without known diabetes was compared to a control group without PCOS or diabetes. In the PCOS group (obese and non-obese), the overall prevalence of IGT and type 2 diabetes was 31.1% and 7.5%, respectively. In the control group, the prevalence of IGT and type 2 diabetes was 14% and 0%, respectively .